to placebo programme

Pain is by the International Association for the Study of Pain defined as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” while “nociception is the neural process of encoding and further processing of noxious stimuli”. Our understanding of nociceptive processing and of the resulting plastic changes after persistent noxious input has increased considerably within the last two decades. It is now clear that long-lasting noxious stimulation or damage to the nervous system give rise to a neuronal hyperexcitability and that this sensitisation of the nervous system plays an important role for development and maintenance of chronic pain. The manifestations of such hyperexcitability are several and include among others: increased neuronal response to a suprathreshold stimulus, expansion of the peripheral areas from where a central neuron can be activated and the recruitment of previous non-responding nociceptive neurons. Furthermore it has been possible to modulate this neuronal hyperexcitability by the discovery of molecular targets for pain, by sequencing DNA of ion channels and receptors and by development of new molecules that can modulate the pain message. The nervous system changes after noxious stimulation or injury and this change in responsiveness appear to be partly time and intensity dependent and partly dependent on the cause of injury. While relative short-lasting and moderate noxious input leads to reversible plastic changes more intense and long-lasting noxious stimulation implies a risk for persistent and more profound changes in transmitters, receptors ion channels and in neuronal connectivity. These changes are seen not only at the level of the first synapse in the spinal cord but also at multiple sites upstream.